The classic theory of specific nerve energies proposes that sensory information is encoded and transmitted centrally along labeled lines. According to this view, the cutaneous sensory modalities of touch, pain, temperature (warmth, cooling) and itch are encoded by specific classes of peripheral neurons and are transmitted by particular central nervous system pathways. Experimental evidence reveals little overlap of adequate stimuli between axons in different sensory categories. For example, nociceptors fail to respond to low intensity thermal and mechanical stimuli while mechanoreceptors are exquisitely sensitive to stimuli that fail excite nociceptor neurons. On the other hand, there has been little investigation of whether inflammation related changes in skin are able to alter the function of non-nociceptive peripheral neurons. Reaction of the cutaneous slowly adapting type I (SAI) mechanoreceptor to serotonin and other chemical species has long been known, but was thought to be a novelty having little practical significance. However, recent evidence now suggests a complex interaction between mechanoreceptor function and inflammatory processes such as that exposure to capsaicin produces modulation of SAI mechanoreceptor behavior similar to that induced by axon reflex activation. The progressive release of substance P, nitric oxide, and prostaglandin E2 (as well as histamine and serotonin through mast cell degranulation) appears to modulate SAI mechanoreceptor activity at each stage of the inflammatory process. We propose experiments to systematically investigate the influence of neurogenic inflammation on SAI mechanoreceptors and to use irnmunocytochemical techniques to identify the cellular elements within the touch dome that influence the type I/Merkel cell complex.